Department of Surgery, University of Colorado, Aurora, CO, USA.
Department of Proteomics and Metabolomics, University of Colorado, Aurora, CO, USA.
Am J Surg. 2023 Dec;226(6):790-797. doi: 10.1016/j.amjsurg.2023.07.040. Epub 2023 Jul 28.
The interactions of polytrauma, shock, and traumatic brain injury (TBI) on thromboinflammatory responses remain unclear and warrant investigation as we strive towards personalized medicine in trauma. We hypothesized that comprehensive omics characterization of plasma would identify unique metabolic and thromboinflammatory pathways following TBI.
Patients were categorized as TBI vs Non-TBI, and stratified into Polytrauma or minimally injured. Discovery 'omics was employed to quantify the top differently expressed proteins and metabolites of TBI and Non-TBI patient groups.
TBI compared to Non-TBI showed gene enrichment in coagulation/complement cascades and neuronal markers. TBI was associated with elevation in glycolytic metabolites and conjugated bile acids. Division into isolated TBI vs polytrauma showed further distinction of proteomic and metabolomic signatures.
Identified mediators involving in neural inflammation, blood brain barrier disruption, and bile acid building leading to TBI associated coagulopathy offer suggestions for follow up mechanistic studies to target personalized interventions.
创伤、休克和创伤性脑损伤（TBI）之间的相互作用对血栓炎症反应仍不清楚，需要进一步研究，以实现创伤的个体化治疗。我们假设，对血浆进行全面的组学特征分析，可以确定 TBI 后独特的代谢和血栓炎症途径。
根据是否存在 TBI 将患者分为 TBI 组和非 TBI 组，并进一步分为多发伤或轻度损伤组。采用发现组学方法对 TBI 和非 TBI 患者组的差异表达蛋白和代谢物进行定量分析。
与非 TBI 相比，TBI 组在凝血/补体级联和神经元标志物方面表现出基因富集。TBI 与糖酵解代谢物和结合型胆汁酸的升高有关。将 TBI 与多发伤进行分组显示，其在蛋白质组学和代谢组学特征上存在进一步的差异。
确定了涉及神经炎症、血脑屏障破坏和胆汁酸生成的中介物，这些中介物导致 TBI 相关的凝血功能障碍，为后续的靶向个体化干预的机制研究提供了建议。
